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J. W. Antoon, M. D. White, E. M. Slaughter, J. L. Driver, H. S. Khalili, S. Elliott, C. D. Smith, M. E. Burow and B.S. Beckman, “Targeting NFκB Mediated Breast Cancer Chemoresistance through Selective Inhibition of Sphingosine Kinase-2,” Cancer Biology & Therapy, Vol. 11, No. 7, 2011, pp. 678-689. doi:10.4161/cbt.11.7.14903
has been cited by the following article:
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TITLE:
Estrogen Receptor Alpha 36 Gene Knockdown Promote the Expression of NF-κB in PC12 Cells
AUTHORS:
Ping Zou, Chao Qu, Yihui Xu, Hongyan Li, Dannv Han, Dan Shi, Wei Zou
KEYWORDS:
NF-κB; Estrogen Receptor Alpha 36; PC12 Cells
JOURNAL NAME:
Open Journal of Endocrine and Metabolic Diseases,
Vol.3 No.4B,
August
6,
2013
ABSTRACT: The nuclear
transcription factors κB (NF-κB) is widely existing in various kinds of cell
types in the nervous system and plays an
important role in neuron apoptosis and neurodegenerative diseases. Estrogen
receptor alpha 36 (ER-α36), is a novel
variant of ERα (as known ER-α66) which can transduce both estrogenand
antiestrogen-dependent activation of MAPK signal pathway and stimulate cell
growth. Here, we aimed to detect the
effect of ER-α36 gene silencing on
the expression of NF-κB in normal cultured PC12 cells and to provide an experimental
foundation for understanding the function of ER-α36 innerve
cells. PC12 cells with ER-α36
expression knocked down by the shRNA method. Then Western blot and immunocytochemical
staining were performed to detect the expression and
translocation of NF-κB after transfection. The results showed that NF-κB
expression was significantly higher comparing with the control group after
transfection (P 0.01). Also, NF-κB subunit entered nuclear after
transfection; Immunofluorescence staining and immunocytochemical staining of
PC12 cells demonstrated that ER-α36
was expressed mainly on the plasma membrane and on the cell nucleus membrane.
These data indicate that ER-α36 gene
silencing can increase the expression of NF-κB and promote its nuclear
translocation in PC12 cells.